Effect of Hemorrhagic Shock on the Reactivity of Resistance and Capacitance Vessels and on Capillary Filtration Transfer in Cat Skeletal Muscle

Abstract

During hemorrhagic shock there is impairment, and eventually abolition, of the responses of both the resistance and the capacitance vessels in cat skeletal muscle to regional lumbar sympathetic vasoconstrictor nerve fiber stimulation and to close intra-arterial infusion of l -norepinephrine. The rate of decline of reactivity is faster, and the time to abolition shorter, for the resistance response than for the capacitance response. Also, the pre-capillary resistance response declines faster and is abolished earlier than the post-capillary resistance response. This impairs and eventually abolishes the ability of constrictor nerve stimulation to decrease mean capillary hydrostatic pressure, and, thereby, causes a net inward movement of extravascular fluid. Preservation of the post-capillary response beyond that of the pre-capillary results eventually in a net outward movement of capillary fluid on nerve stimulation. Replacement of the shed blood restores vascular reactivity to normal. This can occur even when nerve stimulation results in a net loss of capillary fluid, but may not, if this period of shock has been very long. The evidence indicates that pre-capillary functions (small arteries, arterioles, and pre-capillary sphincters) are more under the influence of local metabolic factors than of extrinsic nervous influence. On the other hand, post-capillary functions (post-capillary resistance vessels, and main capacitance vessels) are more dominated by extrinsic nervous influence. However, even in this section the nervous influence may be overcome by relatively large concentrations of "metabolites" as is seen late in the period of hemorrhagic shock. From the results obtained here, it is suggested that early in hemorrhagic shock the sympathetics, at least with respect to skeletal muscle, act in a compensatory manner by maintaining "venous return" (maintained capacitance response) and by increasing circulating blood volume (inward movement of extravascular fluid). The dominant action of local dilator factors on pre-capillary functions has the effect of limiting the magnitude of nerve-induced increased resistance to blood flow and, by impairing the reactivity of the pre-capillary sphincters, distributes the available blood flow over a greater than normal fraction of the capillary bed. Late in the course of hemorrhagic shock, with abolition of pre-capillary responses, the action of the sympathetics would appear to be decompensatory, in that they cause a loss of fluid from the capillaries. This phenomenon may provide a partial explanation for the observed beneficial effect of sympatholytic agents in hemorrhagic shock. The sequence of deteriorating vascular reactivity in skeletal muscle, while not necessarily representative of all tissues, serves to explain many of the hitherto puzzling features of the peripheral vasculature in shock. It also suggests a mechanism, common to all states with reduced tissue blood flow, that may explain lack of response to treatment.